Th17 development is induced by an increase in signal transducer and activator of transcription-3 (STAT3) and a decrease in its inhibitor, suppressor of cytokine signaling inhibitor-3 (SOCS3), which leads to the induction of ROR-γt, thus causing an imbalance of Treg/Th17 populations and maintaining the chronic inflammatory microenvironment that favors cancer development [180]. The gene discussed is STAT3; the disease is cancer.